Rheumatoid arthritis (RA) is characterized by synovial joint inflammation and
destruction. Significant attention is placed on early, aggressive intervention to reduce severity of
disease with induction of remission as the primary goal. However, cardiovascular disease
(CVD) is the main cause of mortality in rheumatoid arthritis patients, accounting for as much as
50% of all reported deaths. The risk for cardiovascular disease in RA is significantly
increased versus the general population and often undertreated, leading to a decrease in life
expectancy. In RA, traditional and novel risk factors along with certain prescribed and overthe-
counter medications play a role in the development and exacerbation of CVD. The
following article will focus on the pathophysiology of CVD in RA, guidelines for identifying
CVD risk in RA patients, and the current treatment options available.

The Pathophysiology of Cardiovascular Disease in Rheumatoid Arthritis
Cardiovascular disease is an inflammatory disorder causing endothelial injury and
dysfunction. Smoking, hypertension, and diabetes along with increased levels of modified lowdensity
lipoprotein (LDL) have been implicated as factors that cause endothelial dysfunction.9
Endothelial injury caused by traditional risk factors leads to an increase in adhesion molecules
(vascular cell adhesion molecule , intercellular adhesion molecule), allowing for the passage
of monocytes into the artery wall. Macrophages are produced in response to monocytes
uptake of oxidized LDL trapped inside the artery wall. Furthermore, macrophages transform
into foam cells after scavenging LDL. Modified LDL in the arterial wall continues to attract
macrophages and T cells, causing an increase in cytokines, chemokines and growth factors to
perpetuate the inflammatory cycle, leading to plaque development and future cardiovascular
events.